Wednesday, August 15, 2012

There Is More Than One Jacques Pepin

(The title is intended to raise a question in your mind. Two men named Jacques Pepin? Who are they, and why do I care? Read on and I'll explain.

The first Jacques Pepin is a world-renowned chef, born in 1935 in Lyon, France. Much of what he is famous for is his work with the late Julia Child, known for "The French Chef" television series on American public television during the 1960's and 1970's. They also collaborated on a number of other programs shown on public television up into the late 1990's and into the beginning of the 21st century. Julia Child passed away in 2004, and today would have been her 100th birthday.

The other is Jacques Pepin, MD, a Canadian infectious diseases specialist from the University of Sherbrooke in Quebec. Arguably, he is not as well known as the chef he shares his name with [I have had to clarify that in conversations I have had with people about this subject], but he should be. He wrote a book, published in October 2011, entitled, "The Origins of AIDS." I read it during winter break and it both intrigued and inspired me to ask more questions. An opportunity was presented during the second semester to do research on a topic in a prescribed manner, and I took that opportunity to research and write the research paper found below. I will be the first person to say that I barely scratched the surface with this effort, but I had a limited canvas to work with. No more than five double-spaced pages and four academic references out of the PubMed databases. There is no doubt that given more time and space, I could have produced a paper considerably more detailed and at least double the number of pages formatted in single spacing. But this work was worth the time and effort I put into it.

The other question you may be asking is "what do they have to do with each other?"  Strictly speaking, absolutely nothing. That said, I remember being asked once when I mentioned Dr. Pepin's book if I was talking about the chef, and I had to direct the person asking towards the book itself. It got their attention as well, and made them nearly forget about the chef for a while. 

On a side note, Sherbrooke is maybe a 3 hour drive from Manchester. I've been there numerous times, long before a U.S. Passport was required to cross the Canadian border. It's a great little city. And the best part was nobody treated me poorly because I don't speak French.....  --WT)

How Did HIV/AIDS Jump to Humans?
Walter Trachim, NREMT-P
April 3, 2012

There has been considerable debate over where the Human Immunodeficiency Virus (HIV) and Acquired Immune Deficiency Syndrome (AIDS) originated from. The debate has been going on since the early 1980’s when the disease began appearing in the human population. One of the more prevalent discussions is whether or not it originated in Cameroon, where a known non-human primate source of the virus originates from, or from what is now the Democratic Republic of Congo (DRC), where between 1957 and 1960 a program existed for the development and distribution of the Oral Polio Vaccine (OPV) (Parris, 2007). Extensive investigation has been carried out on this program to determine whether or not OPV was the source of HIV in Africa, and much has been written to both support and debunk this argument. Additionally, because of the manner in which HIV presents itself, it appears to have characteristics consistent with that of a hybrid virus, much like the virus known as Adeno-SV40 where cells of monkeys and humans are combined and human viruses replicate in monkey cells (Melnick, 2008).

Because of the debate that exists, and the controversy that often surrounds it, many questions are asked about the virus and how it has spread world-wide. But fundamental questions remain: where did HIV/AIDS truly originate from, and how long ago did it surface in humans? Did HIV and AIDS emerge at the same time? And does it have the ability to appear to be different than what it is? Is it an adenovirus?

First, the retrovirus appears not to be an adenovirus. It is part of the genus Lentivirus and is closely related to a virus from this group known as Visna, a virus common to sheep. Other viruses similar to Visna have been found in primates; the origin of these viruses in primates is not known. Two of these viruses are thought to be the ancestors of the group of viruses that make up the Simian Immunodeficiency Virus (SIV), and multiple variants of SIV are believed to be the ancestors of the two main HIV strains: HIV-1 and HIV-2 (Sharp, 2010).

HIV-1 has been divided into three groups that make up its genetic forms:
  • M – Major – this is the most common, and most virulent, strain of HIV-1 found in humans. There are 9 subtypes associated with group M 
  • N – New 
  • O – Outlier 
In addition, there are 6 known sub-subtypes and multiple recombinant types of the virus also associated with HIV-1 (Bartolo et al., 2009). HIV-2, on the other hand, has only two main groups, A and B, which have spread across the human population (Sharp, 2010).

HIV-1 group M is known to have come from the SIV strain restricted to chimpanzees (Pan troglodytes troglodytes) found in parts of Cameroon. Additionally, this form of the virus is also found in green monkeys (Chlorocebus sabaeus), where its infection has been found to be non-pathogenic. Through the use of molecular clocks, it has been found that group M viruses have a common ancestor dating to approximately 1927. Two strains that are related to the 1927 finding but do vary somewhat date to sometime during 1960 (Sharp, 2010; Bartolo et al., 2009). 

It was during the 1920’s that a clinical trial was being held in the Leopoldville laboratory, located in what is now the DRC, of a medication called Pamaquine. This medication was used at that time for the treatment of Trypanosomiasis, commonly known as African sleeping sickness. Many of the patients travelled to the laboratory and the adjacent clinic from Cameroon, where approximately 115,000 people over this period were screened and treated for the presence of the parasite Trypanosoma brucei. The process of screening and treatment required patients to receive multiple infusions and injections – with needles and syringes that were re-used and not properly disinfected - and it is believed that a group of children that were patients during the period of February to July 1927 were some original carriers of HIV-1 group M. In turn, the infection spread to many of the patients seen in this clinic (Parris, 2007). This is significant because it indicates that HIV-1 group M likely originated in Cameroon, not in the DRC. Further research has found that group M came out of the SIV strain infecting chimpanzees that were located in Cameroon (Bartolo et al., 2009).

HIV-2, however, has a different origin than HIV-1. There are two groups, A and B. Both have been traced back to a type of monkey known as the sooty mangabey (Cercocebus atys). It is found mainly in west Africa, and its discovery was first reported in 1989. HIV-2 has been found to be more common among people living in this region than it is in any other location world-wide, and it appears to not have the level of virulence HIV-1 group M has (Sharp, 2010).

Regarding the spread of HIV-1, it has been successful due to much of the activity that has occurred in west and central Africa. Unrest in Angola was a contributing factor, and two contributing events have often been cited. The first is related to the presence of military personnel from Cuba deployed to Angola between 1961 and 1974. The second is civil war that occurred between 1974 and 2002 and the subsequent movement of refugees from Angola to Portugal during that period of time. Because of the prevalence of HIV in both destination countries and the further spread to their surrounding neighbors, these are thought to be seminal events causing HIV to become widespread (Bartolo et al, 2009).

Transmission of SIV from primates to humans has occurred likely through multiple vectors. The most common, and most logical, appears to be through predation. It has been shown that chimpanzees will hunt monkeys, including mangabeys, and it has also been shown that humans will hunt chimpanzees and monkeys. Both of these species are part of a larger indigenous food source that is commonly known as “bush meat.” Considering the process of hunting, killing, and dressing game – any kind of game – it would make sense that body fluids coming from the animals could mix with human fluids (i.e., blood – being cut with machetes, knives, or other sharp objects), potentially creating a source of infection. From this scenario, it is surmised that this is a likely route of SIV into humans (Sharp, 2010).

On the existence of AIDS, evidence exists pointing to the possibility that it existed before HIV. In humans that are positive for the presence of HIV, the likelihood of becoming sick with AIDS is extremely high. The reason for this is not due to the syndrome per se but from the opportunistic infections that overwhelm the immune system. This has also been found to be true in a group of chimpanzees located at the Gombe National Park in Tanzania. In studies that have been performed on this group since 2001, it has been found that in SIV-positive chimpanzees the CD4+ T-cell count is notably lower than in SIV-negative chimpanzees. This is a primary symptom in humans when AIDS is present, and those chimpanzees found to have the lowest CD4+ T-cell counts were strikingly similar to humans with end-stage AIDS. Further research has found that the strain of SIV that these chimpanzees were infected with was a recombinant strain originating from two different species of monkeys, the red-capped mangabey (Cerocebus torquatus) and the greater spot-nosed monkey (Cercopithecus nicitans). Distinct similarities were found in the genomes of the SIV strains of both of these monkeys compared to the SIV strain of the chimpanzees at Gombe: the 5’ end of the chimpanzee genome was nearly identical to that of the mangabey, and the 3’ end to that of the spot-nosed monkey. Additionally, proteins found in the genomes of these monkeys have an effect on their ability to not cause a high-level immune response involving the activation of their T-cells. When the genomes recombined in chimpanzees, however, it appears that this genetic switch was changed, and the immune response that activates T-cells was enabled in the presence of SIV (Sharp, 2010).

 At this point, the original questions need to be asked again:
  • Where did HIV/AIDS truly originate from, and how long ago did it surface in humans? 
  • Did HIV and AIDS emerge at the same time? 
  • Is it an adenovirus? 
In summary, the following are basic answers to the questions raised at the beginning of this paper: 

First, although there is no absolute way to confirm this due to the lack of information available, HIV appears to not be an adenovirus. Rather, it is believed to be a member of the Lentivirus family, where sheep are most often believed to be a source. Additionally, HIV is broken into two distinct virus types, HIV-1 and HIV-2. HIV-1 has been found to have three subtypes of its own, Group M, N, and O. Group M is the most virulent of these as well as those of HIV-2, with a molecular clock origin from around the year 1927. Some of the other subgroups have been found to originate around 1960.

Second, the OPV program run from 1957-1960 is not believed to be responsible for the jump from apes to humans. Rather, the conditions surrounding predation and butchering of game, specifically the transmission of body fluids from apes to humans during this process, is believed to be mostly responsible for the jump to have happened.

Third, unrest and civil war in Angola between 1961 and 2002 is believed to have been a major contributing factor to the spread of HIV/AIDS to other parts of the Western Hemisphere. This is believed to be due to the numbers of foreign military personnel, mainly from Portugal and Cuba, that were deployed to Angola during this time.

Finally, due to a condition that exists in some non-primate monkeys, it is thought that AIDS may have actually existed before HIV. It does not appear to cause an immune-system response in the monkeys but does appear to in some chimpanzees due to genetic switching in a recombined version of SIV.


Bartolo, I., Rocha, C., Bartolomeu, J., Gama, A., Marcelino, R., Fonseca, M.,… & Taviera, M. (2009). Highly divergent subtypes and new recombinant forms prevail in the HIV/AIDS epidemic in Angola: New insights into the origins of the AIDS pandemic. Information, Genetics, and Evolution, 9, 672-682. doi:10.1016/j.meegid.2008.05.003

Melnick, J. (2008). Adeno-SV40 Hybrid Virus. In Access Science. Retrieved from

Parris, G.E. (2007). How did the ancestral HIV-1 group M retrovirus get to Leopoldville from southeastern Cameroon? Medical Hypothesis, 69, 1098-1101. doi:10.1016/j.mehy.2007.02.033

Sharp, P., & Hahn, B. (2010). The evolution of HIV-1 and the origin of AIDS. Philosophical Transactions of the Royal Society, 365, 2487-2494. doi:10.1098/rstb.2010.0031

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